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The Oral Health Implications of Addiction.

© Juliette Reeves 2012

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Abstract

 

 Chemical dependency has many faces and takes many forms, including the use of depressants, stimulants, hallucinogens and alcohol. The most commonly abused substances are caffeine, alcohol and nicotine.  According to the Strategic Taskforce on Alcohol report there is convincing evidence to show that regular consumption of alcohol increases the risk of liver cirrhosis, cancer of the mouth, pharynx, larynx’ oesophagus and liver.  Concurrent abuse of tobacco and alcohol products worsens dental disease and heightens the risk of developing oral cancer.  Many other addictions with oral health implications exist , however, this article will focus on the most common addictions we encounter such as alcohol and nicotine, with a brief look methamphetamines.

Introduction

 

 Chemical dependency has many faces and takes many forms, including the use of depressants, stimulants, hallucinogens and alcohol. The most commonly abused substances are caffeine, alcohol and nicotine. There are a number of Central Nervous System Stimulants (CNSSs) commonly abused by chemically-dependent individuals that include over-the-counter diet pills, prescribed amphetamines, street amphetamines, methamphetamines and cocaine. Many other addictions with oral health implications exist , however, this article will focus on the most common addictions we encounter such as alcohol and nicotine, with a brief look methamphetamines.

 

  According to the Strategic Taskforce on Alcohol report there is convincing evidence to show that regular consumption of alcohol increases the risk of liver cirrhosis, cancer of the mouth, pharynx, larynx’ oesophagus and liver. In a comparison of alcohol consumption and alcohol-related mortality over the last 30 years, increases in cancer, cirrhosis and cardiovascular disease are related to an increase in alcohol consumption.  

 

The prevalence of periodontal disease and caries in alcohol and tobacco dependant patients is high and  exacerbated by a lack of oral hygiene techniques and a  diminished salivary flow. Xerostomia may occur due to nutritional deficiency, enhanced salivary gland apoptosis (1) and psychiatric medication.

 

Oral Cancer

 

Oral cancer has been identified as a significant public health threat. It has been defined by the WHO International Classification of Diseases as a malignancy arising within the lips, oral cavity, oropharynx, nasopharynx, hypopharynx, and other sites within lip, oral cavity and pharynx. Oral cancer is the sixth most common cancer in the world, and its prevalence continues to increase globally (2).  The British Dental Health Foundatio (3) reports that  over the past four years cases of oral cancer in the UK have increased by 17%, an increase more rapid than any other cancer. Oral cancer is largely a preventable disease, related to behavioural and lifestyle factors. The aetiology of oral cancer is multifactorial, with alcohol, tobacco products, a diet low in fruit and vegetable intake, and possibly human papilloma virus, the main risk factors considered responsible for inducing this malignancy. (4,5)

 

 Concurrent abuse of tobacco and alcohol products worsens dental disease and heightens the risk of developing oral cancer. It is difficult to ascertain whether the high risk of periodontal breakdown and oral cancer is caused by the effect of general neglect and smoking or the effect of alcohol directly on the oral tissues.  

 

Erosion

 

One other aspect of alcohol abuse is loss of tooth surface due to erosion. There are two factors why this may be so; chemical damage to the tooth surface due to the acidity of the alcohol itself and erosion associated with alcoholism caused by frequent vomiting (6,7). A study of 37 alcoholic patients showed that their teeth had significantly more wear than age- and sex-matched controls (8). The tooth wear was most marked in males and those whose alcohol consumption was continuous rather than in the form of episodic binges. The wear appeared to be erosive in nature, and in 40% of the sample it affected the palatal surfaces of the upper anterior teeth. It is therefore suggested that dental professionals should bear in mind the possibility of chronic alcoholism in cases of unexplained dental erosion

 

Mandibular Osteomyelitis

 

There also appears to be an increased risk of mandibular osteomyelitis following extraction in the alcoholic patient. (9) It has been suggested that depression of the host’s defences, due to alcoholism modifies the response to, and the spread of, this rare but serious infection.  

 

Alcohol and bone density

 

Patients with alcoholic bone disease reveal a marked impairment in bone formation. Ethanol has been shown to reduce proliferation of osteoblasts. The precise mechanism of how alcohol impairs bone density remains to be clearly defined, but there is an increasing body of evidence emerging to suggest that in the human model, alcohol in large amounts is toxic to osteoblasts Alcohol may also directly affect bone density by impairing liver function and altering both vitamin D and calcium metabolism. The consequences of alcohol intake during adolescence is particularly damaging, as peak bone mass is determined at this time.  

 

There is evidence, however, for a positive effect of moderate alcohol consumption on bone. Social drinking has been associated with higher bone mass. Few studies have undertaken thorough investigations into the mechanisms of action of the proposed beneficial effect of moderate alcohol intake on bone density. Possible theories include the stimulation of calcitonin production and the effect of alcohol on endogenous hormone production. Alcohol may increase the adrenal production of androstnedione and its conversion to oestrogen. Whatever the beneficial effects of alcohol on bone density prove to be, they will only be related to moderate alcohol intake.

 

Smoking

 

As dental professionals we are only too aware of the effects of smoking on the periodontium. Tobacco has long been linked to oral cancer and leukoplakia,. Research over the last 20 years has established a firm association between tobacco use and periodontitis, alveolar bone loss and refractory periodontitis.  

 

There is evidence that cigarette smoking exerts both systemic and local effects.  The main effects of smoking to the oral tissues includes:

 

Tobacco smoke contains cytotoxic and vasoconstrictive substances, including nicotine, which has  direct effects on the blood vessels  supplying the gingival tissues. (10)

 

Nicotine adversely affects fibroblast function and readily penetrates the epithelium of the skin and oral mucosa, resulting in impaired tissue turnover, healing and maintenance of the periodontal attachment. (11)

 

Smoking exerts  deleterious effects on bone formation and maintenance.  Nicotine can suppress the proliferation of cultured osteoblasts while stimulating osteoblast alkaline phosphatase activity. (12) 

 

The effects of smoking on the immune system are well documented. These include inhibition of oral neutrophil function, reduced antibody production, impaired phagocytic activity. and alteration of peripheral blood immunoregulatory  T-cell ratios.

 

Tobacco smoking severely depletes the body of important antioxidant micronutrients needed for effective functioning of the host immune response. This is especially so in the case of vitamin C, beta-carotene and alpha tocopherol. Deficiencies in antioxidant micronutrients result in reduced cell numbers in lymphoid tissue and produce functional abnormalities in the cell mediated immune response. (13) Cigarette smoking impairs the antioxidant protective action of vitamin C, glutathione and other antioxidants at tissue level.  This increased rate of lipid peroxidation and reduced antioxidant status will accelerate the rate of destruction of the periodontium and increase the incidence of oral cancer.  

 

Recent study has suggested that dietary antioxidant intake is significantly lower in smokers than non smokers.(14,15)  Smokers had the lowest dietary vitamin C, beta carotene and tocopherol intake and serum levels compared to those who had never smoked.

 

Methamphetamine Use

 

MA is used in pill or powdered form, and can be injected, snorted,  smoked or taken orally.  It is a bitter tasting powder that readily dissolves in beverages. Another common form of the drug is a clear, chunky crystal. This is the form known as “ice” or “crystal meth” and it is smoked in a manner similar to crack cocaine.  

 

Clandestine production accounts for most of the methamphetamine trafficked and abused worldwide. The illicit manufacture of methamphetamine can be accomplished in a variety of ways, but is produced most commonly using the ephedrine / pseudoephedrine reduction method. Methamphetamine is also made from a mix of toxic substances, including over-the-counter cold medicine, fertilizer, battery acid, hydrogen peroxide, anhydrous ammonia (farm fertilizer), lithium (from batteries), paint thinner, ether, drain cleaner and lighter fluid. The oral effects of methamphetamine use, therefore, can be devastating.  

 

Oral Effects of Methamphetamine.  

 

The toxic and caustic ingredients involved in the making of the drug have devastating effects on the oral tissues. The main effects being rampant caries, increased wear associated with bruxism, xerostomia and possibly periodontal disease (16).   Caries Reports have described rampant caries that resembles early childhood caries, this being referred to as “meth mouth”. In 1995 Howe (17) noted the incidence of gross caries was much  higher in children receiving prescribed MA for obesity and attention deficit disorders. By 2002 Shaner (18) was reporting a distinctive pattern of caries in MA users, involving the buccal smooth surface of the teeth and the interproximal surfaces of the anterior teeth. The teeth of MA users have also been described as “blackened, stained rotting, crumbling or falling apart”.(19)   

 

The rampant caries associated with methamphetamine use has been attributed to the acidic nature of the drug, drug induced xerostomia, its propensity to cause cravings for high calorie carbonated beverages and bruxism, and its long duration of action leading to extended periods of poor oral hygiene (20) The type of carious lesions seen in these individuals resembles "radiation decay”. It is large, dark in colour and appears at the cervical one third of the tooth at the gingival margin.  

 

Xerostomia

 

The xerostomic effects of MA have been attributed to the fact that MA as an sympathomimetic amine, acts on a and b adrenergic receptors. The stimulation of a receptors in the vasculature of the salivary glands produces vasoconstriction and reduces salivary flow (21). This reduces the availability of the protective factors found in saliva. Xerostomia has also been attributed to the elevated metabolism and over activity experienced with MA use.   

 

Bruxism

 

Other risk factors associated with MA use include increase bruxism and clenching. Methamphetamine is a neurotoxin and potent stimulant, which can also cause cerebral oedema and haemorrhage, paranoia and hallucinations. Short-term effects include insomnia, hyperactivity, decreased appetite, increased respiration and tremors, and drug induced grinding (22).   A distinct pattern of tooth wear has been reported in MA users. Richards (23) et al noted that users who preferentially snorted MA had significantly higher tooth wear in the anterior maxillary teeth than patients who injected, smoked, or ingested it. It was suggested that patients who use MA have distinct patterns of wear based on route of administration, the difference being explained anatomically.  

 

Periodontal Disease

 

There is some debate whether these drugs directly contribute to periodontal disease, or whether patient neglect or apathy is the primary cause. The amphetamine Cocaine is known to cause small vessel vasoconstriction which retards the healing process which would, therefore be a factor in the progression of periodontal disease. An increased risk of xerostomia and anorexia caused by the drugs are also deemed to be predominant risk factors in the development of periodontal disease.

 

Conclusion

 

Chemical abuse is a serious national problem that has the potential to affect all of our lives. As dental health professionals, we need to be aware the systemic and oral health effects of drug abuse and how to recognise the oral health risks and provide safe and  adequate treatment. Identification of the substance-abusing patient plus a cancer-screening examination, preventive dental education, and use of saliva substitutes and anticaries agents are indicated. Special precautions must be taken when performing surgery and when prescribing or administering analgesics, antibiotics or sedative agents that are likely to have an adverse interaction with alcohol, drugs or psychiatric medication.  

References

 

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2 Moore SR, Johnson NW, Pierce AM, Wilson DF. The epidemiology of mouth cancer: a review of global incidence. Oral Diseases 2000;6(2):65-74.  

 

www.dentalhealth.org.uk  

 

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6 Jarvinen V, Rytomaa I, Meurmann JH. Location of dental erosion in a referred population. Caries Res 1992;26:391-396.

 

7 Bevenius J, L'Estrange P. Chairside evaluation of salivary parameters in patients with tooth surface loss: a pilot study. Aust Dent J 1990;35:219-221.  

 

8 Robb ND, Smith BG: Prevalence of pathological tooth wear in patients with chronic alcoholism. Br Dent J. 1990 Dec 8-22;169(11):367-9.  

 

9 Davies HT, Carr RJ. Osteomyelitis of the mandible: a complication of routine dental extractions in alcoholics. Br J Oral Maxillofac Surg. 1990 Jun;28(3):185-8  

 

10 Raulin. L., McPherson.J., McQuade. M., et al : The effect of nicotine on the attachment of fibroblasts to glass and human root surfaces in vitro.  J. Periodontol. 59(5):318-325. 1989.  

 

11 Hanes. P., Schuster. G., Lubas.S.: Binding, uptake and release of nicotine by human gingival fibroblasts. J. Periodontol. 62:147-152. 1991.  

 

12 Fang. M.A., Frost. P.J., Iida-Klein. A., Hahn. T.J.: Effects of nicotine on cellular function in UMR 106-01 osteoblast-like cells. Bone. 12:283-286. 1991.  

 

13 Grimble. R.F.: Effect of antioxidative vitamins on immune function with clinical applications.  Int. J. for Vit. and Nutr. Res. 67(5):312-20. 1997.  

 

14 Zondervan. K.T., Ocke.M.C., Smit. H.A., Seidell. J.C. : Do dietary and supplementary intakes of antioxidants differ with smoking status? Int J Epidemiol. 25(1):70-9. Feb 1996  

 

15 Schectman.G., Byrd.J.C., Gruchow.H.W.: The influence of smoking on vitamin C status in adults. Am J Pub Health 79(2):158-62. Feb 1989  

 

16 Klasser GD, Epstein J: Methamphetamine and its impact on dental care. J Cand Dent Assoc 2005: 71(10): 759-62.  

 

17 Howe AM. Methamphetamine and childhood adolescent caries. Aust Dent J. 1995 40(5) 340.  

 

18 Shaner JW. Caries associated with methamphetamine abuse. J Mich Dent Assoc. 2002 Sept;84(9):42-7.  

 

19 American Dental Association: ADA warns of methamphetaime’s effect on oral health. 2 Aug 2005 www.ada.org/public/media/releases/0508-release 01.asp  

 

20 McGrath C, Chan B. Oral health sensations associated with illicit drug abuse. Br Dent J. 2005 Feb 12;198(3):159-62.  

 

21 Physicians’ Desk Reference. 59 ed. Montvale, New Jersey: Thompson PDR; 2005. p2568-9.  

 

22 U.S. National Institute on Drug Abuse. NIDA for Teens. Mind over Matter: Teaching Guide. Available at: http://www.nida.nih.gov/PDF/MOM/TG-Meth.pdf23[1] Richards JR, Brofeldt BT. Patterns of tooth wear associated with methamphetamine use. J Periodontol. 2000 Aug;71(8):1371-4.                             

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